indulge a neophite....curious about your statements on lactate metabolism...
im an engineer (chemical) with a bit of background biology and the like...so i apologize for the possibly silly questions...
I always understood lactic (lactate) levels to have a strong positive correlation with 1) levels of physical activity/rest, and 2) the perception of fatigue and "pain"...Are you saying that 2) is just not true (causal relationship b/i lactate and pain)? from your post you seem to indicate that acification is the main reason for 2), is that right? always thought that pH was tightly regulated (0.1-0.2 pH otherwise many enzymes are not operating in their optimal point) and that you basically had anywhere from about pH 7 to pH 4 (in dedicated compartments) fixed, would excercise change those levels significantly (say by more than 0.5 points?)..
what part of pain perception can be attributed to tissue injury in "normal" excercise vs changes in the chemistry of the tissue? Is the response to injury (if any) post-excercise the reason for increase builtup of muscle tissue, or more of a direct response to mechanical load above "normal" activity...would that go along with the necessity for proper recovery time to allow for tissue builtup rather than continued wear and tear of an alrready "compromised" tissue (actual loss of mass!)? Would it be fair to say that most of this control/regulation is kinetic and NOT thermodynamic (either in terms of mechanical wear vs buildup, and acidification vs buffering (rxn kinetics) and transport across cellular boundaries and waste disposal
)...
On the ATP->ADP you describe, does the proton come from the phosphate group lost? or the ADP, i.e., is there a corresponding change in pKa of ADP vs ATP that would favor release of H+ under physiological pH???
Are you also implying that pyruvate to lactate conversion is one of the main buffering mean of excercise related acidification?...but that would not be consistent with 2) above??? What is, briefly, the relationship bewteen acidification and perception of pain, basically, how do the protons couple with nerve excitation???
Did you guys use tracers to determine the nature of the "lactate species" (for ex. a ionic isotope)? what kind of direct evidenve do you have to claim that lactic acid jsut does not occur in the human body?...what pH is required for the ionic exchange or protonation, what ionic strength is required? the pKa of Lactic acid has probably been known for a long time, along with cellular pH in different places (and roughly the ions concentrations), why does the realisation that only lactate occurs only happens now? am i missing something?? Puzzling...Also the protonation levels of lactate (and balance of salt form) vs pH, as far as I know, show a *distribution* uniquely defined by the pKa(s) so its hard to believe that out of, say, 1 mol of lactate, none of it occurs in its lactic acid form..its not really a "swicth" behavior on or off but a continuous functional relationship...were you just speaking "nominally"? if thats the case, how can you assert that none of the lactic acid (however small that fraction is in relation to lactate) has NO physiological effect...
What of all the research on lactic acid (of which I have very little to no knowledge) and excercise? how many poeple are you guys p...off?
thanks for your reply and time, looking forward to your reply.
dave morris said:
Actually, you can forget most of what you have read about lactic acid (including what you may have read in my book) and throw it out the window. New evidence out of our lab and the University of New Mexico, as well as a couple of others around the world is showing pretty convincingly that the human body is incapable of producing lactic acid - the pH of the human body just won't allow it. Instead, the human body produces lactate (an acid salt of lactic acid). The "acid" that is produced by the body is in the form of free hydrogen ions that cause acidic conditions that, in turn, leads to fatigue. Lactate itself does nothing to contribute to the production of hydrogen. In fact, the conversion of pyruvate to lactate actually consumes hydrogen and delays fatigue. So a retarded ability to produce lactate is actually a disadvantage. Where do the hydrogens come from? Interestingly, the conversion of ATP to ADP (the chemical reaction that releases energy for contracting muscle) is a major source of hydrogen ions.
As far as Lance is concerned, I've tested the guy and he produces lactate at a level that is consistent with other elite road cyclists, he just tends to be able to produce more power before he accumulates hydrogen ions.
Your symptoms are something I have seen in some others. While I am not sure what is behind the burning, I am sure that you will increases your working capacity by performing short, high-intensity intervals (leadout intervals if you have read my book) a couple of times a week.
best of luck,
Dave
